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Background and aims Endothelial dysfunction, insulin resistance and oxidative stress are believed to be central and associated mechanisms in atherogenesis. We aimed to determine the effect of the antioxidant vitamin E on endothelial function, insulin action and cardiovascular risk markers in young healthy adult offspring of parents with Type 2 diabetes. Methods Healthy, glucose-tolerant adults (18–38 years), 14 (12 male/2 female) with at least one parent with Type 2 diabetes, and 14 (12 male/2 female) subjects with no family history of diabetes (controls) were studied. Insulin action was assessed by euglycaemic hyperinsulinaemic clamp (1 mU/kg/min). Endothelial function was assessed by forearm blood flow (FBF) responses to intra-brachial artery infusions of acetylcholine (ACh) (endothelium-dependent vasodilation), sodium nitroprusside (SNP) (endothelium-independent vasodilation) and NG-monomethyl l-arginine (LNMMA) (nitric oxide synthase inhibition). Thirteen offspring (18–38 years, 11 male/2 female, BMI

Objective: Estrogen deficiency is associated with increased cardiovascular risk and endothelial dysfunction. Improvements in endothelial function with antioxidants, including vitamin C, have been reported. We aimed to determine the acute effect of vitamin C on endothelial function in healthy women with established menopause. Subjects: Subjects (aged 47-59 years) were at least 1 year postmenopause. Ten (serum estradiol < 50 pmol/l) were not receiving hormone replacement therapy, while eight hysterectomized subjects received subcutaneous estradiol. Design: Forearm blood flow (FBF; strain-gauge plethysmography) responses to intrabrachial artery infusions of incremental doses of acetylcholine (endothelium-dependent vasodilation) and sodium nitroprusside (endothelium-independent vasodilation) were determined at baseline, and following 1.5 g vitamin C given intravenously. Results: At baseline, estrogen-treated subjects had a lower index of insulin resistance (homeostasis model assessment, HOMA) and lower fibrin...

C CLARKE, CG BRENNAN, K RODGERS, RM DWYER, PPA SMYTH ENDOCRINE LABORATORY, DEPARTMENT OF MEDICINE AND THERAPEUTICS, UNIVERSITY COLLEGE DUBLIN, IRELAND he demonstration in extrathyroidal human tissues of the sodium iodide symporter (NIS) has raised the possibility that 1311, commonly used as a systemic therapeutic ablative agent in hyperthyroidism and thyroid cancer, might be applied in the treatment of tumours in other NISexpressing tissues such as human breast cancer. Thyroidal transport of 1311 is known to be proportional to circulating stable I and the aim of this study was to determine how stable I (KI) would effect such transport in human breast cancer cell lines MDA-MB-231, MCF-7 and in FRTL-5 thyroid cells. All cells were incubated with KI (01 00mM) for 72 hours after which 1Th I was added . Incubation and uptake of 'l by cells was counted every four hours. Timed efflux of '^I was measured every five minutes. KI in the incubation medium blocked 1251 uptake in a dose-dependent manner in the E receptor positive MCF7 cell line. The effect was less marked in the E receptor negative MDA-MB-231 with significant uptake being maintained even at an I concentration of 50mM. A similar blockade was seen in the FRTL-5 cells with maximum uptake blockade of 25mM I. The rate of efflux of 15I was similar in both MCF-7 and MDA-MB-231 cell lines with a tin of 35 and 40 minutes respectively. In contrast, efflux from the FRTL-5 cells was faster (tire=15 mins). As the human breast has a much lower avidity for I than the thyroid, control of dietary intake would assume even greater importance in radioactive iodine treatment of breast tumours or their metastases.